Horm Metab Res 2008; 40(1): 60-65
DOI: 10.1055/s-2007-993170
Humans, Clinical

© Georg Thieme Verlag KG Stuttgart · New York

Relationship between Endogenous Parathyroid Hormone and Bone Metabolism/Geometry in Female Patients Treated with Glucocorticoid

H. Kaji 1 , M. Yamauchi 2 , K. Chihara 1 , T. Sugimoto 2
  • 1Division of Diabetes, Metabolism and Endocrinology, Department of Internal Medicine, Kobe University Graduate School of Medicine, Chuo-ku, Kobe, Japan
  • 2Internal Medicine 1, Shimane University Faculty of Medicine, Izumo, Shimane, Japan
Further Information

Publication History

received 04.12.2006

accepted 24.04.2007

Publication Date:
11 December 2007 (eFirst)

Abstract

Although the role of PTH (parathyroid hormone) has been debated in glucocorticoid (GC)-induced osteoporosis (GIO), clinical data about the relation of endogenous PTH to bone metabolism in patients treated with GC are still lacking. The present study was performed to examine the relationship of PTH to bone metabolic indices, bone mineral density (BMD), and bone geometry in 174 female patients treated with oral GC for more than 6 months. Dual-energy X-ray absorptiometry and peripheral quantitative computed tomography (pQCT) were employed for the assessment of BMD and bone geometry. No elevation of serum PTH levels was observed in patients treated with GC. Although serum levels of osteocalcin were not related to serum PTH levels, urinary levels of deoxypiridinoline were positively correlated. Serum PTH levels were negatively related to BMD at any site. In pQCT, serum PTH levels were negatively correlated to both trabecular and cortical volumetric BMD. As for bone morphometric indices, serum PTH levels were significantly related to endocortical circumferences, cortical thickness, and cortical area. Moreover, serum PTH levels were significantly higher in patients with vertebral fractures, compared with those without vertebral fractures in GC-treated patients. In the present study, serum PTH levels were related to the elevation of bone resorption marker, decreased BMD, cortical thinning, and an increase of vertebral fracture risk. The elevation of sensitivity to PTH in bone might play some role in the pathogenesis of GIO.

References

Correspondence

H. Kaji

Division of Diabetes, Metabolism and Endocrinology

Department of Internal Medicine

Kobe University Graduate School of Medicine

7-5-2 Kusunoki-cho

Chuo-ku

650-0017 Kobe

Japan

Phone: +81/78/382 58 85

Fax: +81/78/382 58 99

Email: hiroshik@med.kobe-u.ac.jp